Fusarium head blight (FHB) is a worldwide disease in cereal crops, causing significant yield losses, grain quality reductions, and the production and accumulation of mycotoxins in the grain. The objective of this work was to analyse the influence of climatic factors on the incidence of FHB, the Fusarium species involved, and the mycotoxin content in wheat across Ireland during 2001, 2002 and 2003. At least ten field sites were selected each year. Two hundred ears of winter wheat were collected randomly at each site at mid-anthesis, milky-ripe stage and at harvest. Visual disease incidence, FHB species and mycotoxin analysis were completed. Temperature, relative humidity (RH), leaf wetness (LW) and rainfall were recorded at each site from early June (mid-anthesis) to the end of August (harvest). Results showed that FHB was present throughout Ireland in each year. There was no significant difference in disease incidence in 2001, 2002 and 2003, indicating that overall disease incidence in the country did not change. Disease severity however, was found to be higher in 2003 than 2002. Species-specific PCR showed that, across the sites, five Fusarium species were detected each year, but the relative abundance of each species varied dramatically. In 2001, F. culmorum was the predominant species and M. nivale var. nivale was the least, whereas M. nivale var. majus was the predominant species detected in 2002 and 2003. Mycotoxin analysis showed that in 2001, deoxynivalenol (DON) was present in all sites; zearalenone (ZON) was detected at 11 out of 12 sites and nivalenol (NIV) was detected in 10 sites. In 2002 mycotoxin incidence was low with DON, ZON and NIV present in less than 5 of the 13 sites. In 2003 DON was present in 7 out of 10 sites, ZON was detected at 3 out of 10 sites and NIV was detected in 1 out of 10 sites. There was no significant correlation between the visual symptoms (average head incidence), the amount of Fusarium (quantitative PCR), and the amount of mycotoxins, implying that mycotoxin accumulation may have occurred in healthy-looking grain. Statistical analysis showed significant correlations between visual symptoms and LW in 2001. Rainfall was significantly correlated with mycotoxin levels in 2001 and 2002.
Development of potato tuber diseases caused by Rhizoctonia solani
Alex Hilton, R Griffin-Walker, S Matheson and SJ Wale
SAC, Craibstone Estate, Aberdeen, Scotland
Rhizoctonia solani AG-3 causes a number of diseases of potato including, stem and stolon canker in the growing crop, black scurf and russetting on the tubers. Stem canker and black scurf are greater where crops are placed under stress but the cause and relationship to crop development and russetting are not understood.
In a field experiment, healthy seed of cv. Desirée was planted in soil artificially amended with mycelia of R. solani. Three levels (Low 100 kg / ha, Medium 180 kg / ha and High 260 kg / ha) of nitrogen fertiliser were added at planting in order to create stress conditions. Once daughter tubers started to develop they were regularly assessed for disease and related to the status of the crop. This monitoring showed that russetting occurred soon after tubers developed but that black scurf did not appear till the canopy had started to senesce. Degree of skin set at harvest was also measured by placing tubers in a rotating scuff barrel and measuring level of skin damage. This revealed significant associations between skin set with both black scurf (r= -0.74) and russetting (r =-0.61). Although russetting and black scurf are both caused by R. solani they behave as two distinct diseases. Early harvesting will reduce the severity of black scurf but not russetting whilst application of nitrogen at planting had no effect on symptom development.
Analysing the risk of brown rot to the Scottish seed potato industry
P. van de Graaf1, J. Danial1, N.M. Parkinson2, J.G. Elphinstone2, G.J. Bryan3 & G.S. Saddler1
1 Scottish Agricultural Science Agency, 82 Craigs Road, East Craigs, Edinburgh EH11 8NJ, UK; 2 Central Science Laboratory, Sand Hutton, York YO4 1LZ, UK; 3 Scottish Crop Research Institute, Invergowrie, Dundee DD2 5DA, UK
The quarantine bacterium Ralstonia solanacearum biovar 2 race 3, the cause of potato brown rot, is known to be present in a number of European waterways, including some English rivers. It was previously detected in parts of the Tay river system but has not been found in Scotland for the past three years. Possible sources of future renewed contamination of Scottish rivers with R. solanacearum could include waste from imported potatoes in sewage and potato processing effluent. Once in the water, the bacterium would be able to survive and multiply in the wild host Solanum dulcamara, which is abundant along the banks of several Scottish rivers and streams. Any surface water contaminated with R. solanacearum used for irrigation would form a major threat to the health of potato crops, and thus to the Scottish seed potato industry. For this reason, SASA, in co-operation with CSL and SCRI, is currently analysing the risk of brown rot to Scottish seed potato crops in a three-year SEERAD funded project. Within the project, river systems are assessed on the likelihood of contamination with R. solanacearum and the chances of pathogen spread and survival. Infection and disease development are studied under conditions most likely to occur in the field in Scotland, such as low temperature and low inoculum level. The most commonly grown Scottish seed varieties are tested for their susceptibility to the pathogen under these conditions. Methods for the detection of R. solanacearum in water samples are improved to ensure more sensitive and thus faster discovery of the pathogen in Scottish waterways. The chances of pathogen survival and infection of potato crops could also be linked to the genetic variation in both the pathogen and its wild host, S. dulcamara. The molecular tools MLST and AFLP are being used to determine the genetic variation in different strains of R. solanacearum biovar 2 race 3 and in Scottish populations of S. dulcamara respectively. Any genetic differences found might be linked to differences in pathogenicity between strains of the bacterium or in susceptibility of different varieties of its wild host.